Editing Exercise physiology (section)

=== Other ===
* Plasma [[catecholamine]] concentrations increase 10-fold in whole body exercise.<ref>{{Cite journal |last=Holmqvist |first=N |last2=Secher |first2=NH |last3=Sander-Jensen |first3=K |last4=Knigge |first4=U |last5=Warberg |first5=J |last6=Schwartz |first6=TW |year=1986 |title=Sympathoadrenal and parasympathetic responses to exercise |journal=Journal of Sports Sciences |volume=4 |issue=2 |pages=123–8 |doi=10.1080/02640418608732108 |pmid=3586105}}</ref>
* [[Ammonia]] is produced by exercised skeletal muscles from ADP (the precursor of ATP) by [[AMP deaminase|purine nucleotide deamination]] and [[amino acid]] [[catabolism]] of [[myofibrils]].<ref name="Nybo, L. 2005">{{Cite journal |last=Nybo |first=L |last2=Dalsgaard |first2=MK |last3=Steensberg |first3=A |last4=Møller |first4=K |last5=Secher |first5=NH |year=2005 |title=Cerebral ammonia uptake and accumulation during prolonged exercise in humans |journal=The Journal of Physiology |volume=563 |issue=Pt 1 |pages=285–90 |doi=10.1113/jphysiol.2004.075838 |pmc=1665558 |pmid=15611036}}</ref>
* [[interleukin-6]] (IL-6) increases in blood circulation due to its release from working skeletal muscles.<ref>{{Cite journal |last=Febbraio |first=MA |last2=Pedersen |first2=BK |year=2002 |title=Muscle-derived interleukin-6: Mechanisms for activation and possible biological roles |journal=FASEB Journal |volume=16 |issue=11 |pages=1335–47 |doi=10.1096/fj.01-0876rev |pmid=12205025 |s2cid=14024672 |doi-access=free}}</ref> This release is reduced if glucose is taken, suggesting it is related to energy depletion stresses.<ref>{{Cite journal |last=Febbraio |first=MA |last2=Steensberg |first2=A |last3=Keller |first3=C |last4=Starkie |first4=RL |last5=Nielsen |first5=HB |last6=Krustrup |first6=P |last7=Ott |first7=P |last8=Secher |first8=NH |last9=Pedersen |first9=BK |year=2003 |title=Glucose ingestion attenuates interleukin-6 release from contracting skeletal muscle in humans |journal=The Journal of Physiology |volume=549 |issue=Pt 2 |pages=607–12 |doi=10.1113/jphysiol.2003.042374 |pmc=2342952 |pmid=12702735}}</ref>
* Sodium absorption is affected by the release of interleukin-6 as this can cause the secretion of [[arginine vasopressin]] which, in turn, can lead to exercise-associated dangerously low sodium levels ([[hyponatremia]]). This loss of sodium in [[blood plasma]] can result in swelling of the brain. This can be prevented by awareness of the risk of drinking excessive amounts of fluids during prolonged exercise.<ref>{{Cite journal |last=Siegel |first=AJ |last2=Verbalis |first2=JG |last3=Clement |first3=S |last4=Mendelson |first4=JH |last5=Mello |first5=NK |last6=Adner |first6=M |last7=Shirey |first7=T |last8=Glowacki |first8=J |last9=Lee-Lewandrowski |first9=E |last10=Lewandrowski |first10=Kent B. |display-authors=8 |year=2007 |title=Hyponatremia in marathon runners due to inappropriate arginine vasopressin secretion |journal=The American Journal of Medicine |volume=120 |issue=5 |pages=461.e11–7 |doi=10.1016/j.amjmed.2006.10.027 |pmid=17466660}}</ref><ref>{{Cite journal |last=Siegel |first=AJ |year=2006 |title=Exercise-associated hyponatremia: Role of cytokines |journal=The American Journal of Medicine |volume=119 |issue=7 Suppl 1 |pages=S74–8 |doi=10.1016/j.amjmed.2006.05.012 |pmid=16843089}}</ref>